This is a multi-center, randomized, multi-dose, dose-escalation study designed by Dr. Krueger and his collaborators at other universities. The objective is to define the relationship of tolerability to the dose and plasma concentration of a unique pharmacologic agent, BG9712, administered once weekly for twelve weeks to subjects with moderate to severe plaque psoriasis. Psoriasis is an inflammatory disorder of the skin, characterized by hyperproliferation of the most superficial layers of the skin (the epidermis) and inflammation of this layer. The inflammatory nature of psoriasis is mediated by activated T-lymphocytes and antigen-presenting cells at the dermal-epidermal junction of the skin. Migration of these cells into the area occurs before the hyperproliferation begins. Clinical studies have indicated that regression of psoriatic plaques is proceeded by a depletion of epidermal T-cells. Injection of activated human T-cells into mice carrying grafts from uninvolved sites of skin from patients with psoriasis results in the development of psoriatic plaque lesions in the engrafted skin. Similar injections into grafts of normal skin do not produce this effect. Activation of T-cells requires at least two signals. The first is a signal driven by engagement of the T-cell receptor with antigen. The second signal, designated a co-stimulatory signal, results from the engagement of a costimulatory ligand on the antigen-presenting cell, with its receptor on the T-cell. A key costimulatory signal is provided by the interaction of the T-cell receptor CD2 with its ligand, LFA-3, which is on the antigen-presenting cell. The hypothesis underlying this study is that the unique fusion protein (LFA-3/IgG1) can block T-cell activation in psoriatic skin lesions. This study builds upon earlier studies done by Dr. Krueger on the GCRC with BG9712. The original phase I toxicity studies with the drug were carried out here, and now efficacy and pharmacokinetic studies are planned.